ArticleAddiction biology2016
Methamphetamine induces a rapid increase of intracellular Ca(++) levels in neurons overexpressing GCaMP5.
Article in Addiction biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 16 citations in OpenAlex.
- Molecular Mechanisms of Hippocampal Synaptic Plasticity Disruption Induced by Chronic Methamphetamine Exposure: A Narrative Review.Cellular and molecular neurobiology · 2026Review
- AAV-Mediated Expression of Methamphetamine Monoclonal Antibody Attenuates Methamphetamine Behaviour Sensitization in Mice.Addiction biology · 2025Article
- Article
- Methamphetamine Dysregulation of the Central Nervous System and Peripheral Immunity.The Journal of pharmacology and experimental therapeutics · 2021Review
- The Role of α-Synuclein in Methamphetamine-Induced Neurotoxicity.Neurotoxicity research · 2021Review
- Human Milk Oligosaccharide 2'-Fucosyllactose Reduces Neurodegeneration in Stroke Brain.Translational stroke research · 2020Article
- Methamphetamine increases dopamine release in the nucleus accumbens through calcium-dependent processes.Psychopharmacology · 2020Article
- Post-treatment with Posiphen Reduces Endoplasmic Reticulum Stress and Neurodegeneration in Stroke Brain.iScience · 2020Article
- Methamphetamine Activates Trace Amine Associated Receptor 1 to Regulate Astrocyte Excitatory Amino Acid Transporter-2 via Differential CREB Phosphorylation During HIV-Associated Neurocognitive Disorders.Frontiers in neurology · 2020Article
- Pifithrin-Alpha Reduces Methamphetamine Neurotoxicity in Cultured Dopaminergic Neurons.Neurotoxicity research · 2019Article
- Neurotrophic and neuroprotective effects of oxyntomodulin in neuronal cells and a rat model of stroke.Experimental neurology · 2017Article
- Differential modulation of methamphetamine-mediated behavioral sensitization by overexpression of Mu opioid receptors in nucleus accumbens and ventral tegmental area.Psychopharmacology · 2016Article
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
In this study, methamphetamine (Meth)- and glutamate (Glu)-mediated intracellular Ca(++) (Ca(++) i) signals were examined in real time in primary cortical neurons overexpressing an intracellular Ca(++) probe, GCaMP5, by adeno-associated viral (AAV) serotype 1. Binding of Ca(++) to GCaMP increased green fluorescence intensity in cells. Both Meth and Glu induced a rapid increase in Ca(++) i, which was blocked by MK801, suggesting that Meth enhanced Ca(++) i through Glu receptor in neurons. The Meth-mediated Ca(++) signal was also blocked by Mg(++) , low Ca(++) or the L-type Ca(++) channel inhibitor nifedipine. The ryanodine receptor inhibitor dantrolene did not alter the initial Ca(++) influx but partially reduced the peak of Ca(++) i. These data suggest that Meth enhanced Ca(++) influx through membrane Ca(++) channels, which then triggered the release of Ca(++) from the endoplasmic reticulum in the cytosol. AAV-GCaMP5 was also injected to the parietal cortex of adult rats. Administration of Meth enhanced fluorescence in the ipsilateral cortex. Using immunohistochemistry, Meth-induced green fluorescence was found in the NeuN-containing cells in the cortex, suggesting that Meth increased Ca(++) in neurons in vivo. In conclusion, we have used in vitro and in vivo techniques to demonstrate a rapid increase of Ca(++) i by Meth in cortical neurons through overexpression of GCaMP5. As Meth induces behavioral responses and neurotoxicity through Ca(++) i, modulation of Ca(++) i may be useful to reduce Meth-related reactions.
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